Abstract
Mast cells (MCs) are densely granulated perivascular resident cells of hematopoietic origin. Through the release of preformed mediators stored in their granules and newly synthesized molecules, they are able to initiate, modulate, and prolong the immune response upon activation. Their presence in the central nervous system (CNS) has been documented for more than a century. Over the years, MCs have been associated with various neuroinflammatory conditions of CNS, including stroke. They can exacerbate CNS damage in models of ischemic and hemorrhagic stroke by amplifying the inflammatory responses and promoting brain–blood barrier disruption, brain edema, extravasation, and hemorrhage. Here, we review the role of these peculiar cells in the pathophysiology of stroke, in both immature and adult brain. Further, we discuss the role of MCs as potential targets for the treatment of stroke and the compounds potentially active as MCs modulators.
Highlights
Mast cells (MCs) are perivascular resident cells of haemopoietic origin distributed in most tissues surrounding blood vessels, nerves, smooth muscle cells, sebaceous and sweat glands, hair follicles, and synovial membranes [1,2]
About 85% of strokes are ischemic, 10% are due to intracerebral hemorrhage, and 5% are caused by subarachnoid hemorrhage [59,60,61]
Carnosine attenuates mastocytic degranulation and histamine release induced by oxygen and glucose deprivation (OGD) [85], suggesting that the MCs stabilizer capability of the molecule can be involved in the beneficial effects observed in preclinical models of brain ischemia
Summary
Mast cells (MCs) are perivascular resident cells of haemopoietic origin distributed in most tissues surrounding blood vessels, nerves, smooth muscle cells, sebaceous and sweat glands, hair follicles, and synovial membranes [1,2]. MCs are more abundant in the anatomical regions in contact with the external environment, including skin, conjunctiva, nasal mucosa, bronchial airway connective tissue, lung intra-alveolar space, mouth, and subserosal and submucosal layers of the gastrointestinal tract [2,3,4]. Brain vascular pathologies, including stroke and cerebral aneurysm (CA), have been described in Hyper-IgE syndrome and DOCK8 deficiency, two genetic disorders characterized by elevated IgE serum levels, recurrent infections, and allergic reactions [28,29,30]. These findings suggest a possible correlation between IgE levels and stroke. We summarized compounds potentially active as MCs modulators in the treatment of stroke
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